Abstract
Glutathione (GSH) is the main non-enzymatic antioxidant playing an important role in detoxification, signal transduction by modulation of protein thiols redox status and direct scavenging of radicals. The latter function is not only performed against reactive oxygen species (ROS) but GSH also has a fundamental role in buffering nitric oxide (NO), a physiologically-produced molecule having-multifaceted functions. The efficient rate of GSH synthesis and high levels of GSH-dependent enzymes are characteristic features of healthy skeletal muscle where, besides the canonical functions, it is also involved in muscle contraction regulation. Moreover, NO production in skeletal muscle is a direct consequence of contractile activity and influences several metabolic myocyte pathways under both physiological and pathological conditions. In this review, we will consider the homeostasis and intersection of GSH with NO and then we will restrict the discussion on their role in processes related to skeletal muscle function and degeneration.
Highlights
IRCCS San Raffaele Pisana, Department of Human Sciences and Promotion of the Quality of Life, Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy
Tight-regulated crosstalk between nitric oxide (NO) and GSH is pivotal for maintaining muscle homeostasis, as they regulate a variety of signaling mechanisms necessary for preserving muscle integrity under as they regulate a variety of signaling mechanisms necessary for preserving muscle integrity under resting and physical exercise stimulation
Starting from the effects of radical species that formerly gave the ascertain of their involvement in muscle functions we damaging effects of radical species that formerly gave the ascertain of their involvement in muscle have the knowledge that reactive oxygen species (ROS)/RNS are fundamental for proper muscle physiology, as part of functions we have the knowledge that ROS/RNS are fundamental for proper muscle redox-mediated signaling pathways, and that derangement in their production participates in muscle physiology, as part of redox-mediated signaling pathways, and that derangement in their aging and dysfunctions
Summary
The P-SNO can be reconverted to systems, P-SH by among which GSH playsamong a prominent role through the translocation reaction of NO that generates thiol-dependent systems, which GSH plays a prominent role through the translocation reaction. Based on this evidence, it is conceivable to link the majority of effects of NO that generates GSNO [18,21] (Figure 2).
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